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Volume 9 Number 4

Guy R. Schenker, D.C.
April, 1998

Dear Doctor,

     You have learned from the last two month's Letters that 
your sympathetic and parasympathetic patients can often 
present with a wildly bizarre conglomeration of physical and 
emotional symptoms.  You have also learned about the power of 
your Quick Reference Guide (QRG) protocol to identify the 
existence of one of these metabolic imbalances in a matter of 
seconds.  Finally, you have gained complete confidence in your 
ability to handle even these most challenging patients with 
Complex S and Complex P plus the specific amino acids and 
other supplements listed in your QRG.

     We closed last month by introducing a discussion of a 
terribly troubling condition -- asthma.  Just what exactly is 
asthma and how does it relate to your NUTRI-SPEC testing 


     Every asthma patient has an over-sensitive, over-reactive
vagus (parasympathetic) nerve into the bronchial tree which is 
causing a tendency to bronchial constriction accompanied by 
excess bronchial secretion.  This facilitated, over-sensitized
state of the vagal innervation of bronchial tissue is the 
underlying cause of the asthma.  In other words, this 
parasympathetic reflex is always very, very close to its 
threshold point.

     To actually precipitate an asthma attack in a vagal 
facilitated patient requires a trigger -- some additional 
irritant to stimulate the vagus to exceed threshold.  That 
trigger can be an upper respiratory infection; it can be an 
allergy; it can be the stress of exercise; it can be an 
additional stimulatory input to the parasympathetic system 
from the neuro-musculo-skeletal system -- such as a 
chiropractic subluxation or TMJ dysfunction; it can be an 
emotional stress; it can be another NUTRI-SPEC metabolic 
imbalance superimposed upon the parasympathetic tendency
                            - 2 -

(-- very commonly an anaerobic or a dysaerobic or an alkaline 

     Once an asthma attack has been triggered, here is the 
sequence of events.  The bronchial tree constricts and 
increases both its serous and mucous secretion.  This causes 
increasingly labored breathing and also triggers a respiratory
inflammatory reaction which brings various prostaglandins into 
the picture.  The increased airway resistance, plus the 
presence of excess fluid, plus the activity of prostaglandins 
causes an inflammatory response and a swelling of the tissues 
which has now progressed to the point of a positive feed-back 
loop.  In other words, the asthma causes irritation of the 
bronchial tree which feeds back afferently to the central 
nervous system and then back over the vagus to the bronchial 
tree, causing more constriction and more secretion and thus 
more inflammation and prostaglandin activity and so on and so 

     To break this positive feed-back loop we, as NUTRI-SPEC 
practitioners, must decrease the underlying parasympathetic 
tone (and increase the antagonistic sympathetic tone), plus do 
whatever we can to eliminate the trigger.  This includes 
correcting any other NUTRI-SPEC fundamental imbalances plus 
the prostaglandin imbalance.

     From a NUTRI-SPEC perspective there is something else 
very interesting going on in these asthma patients.  Because 
an asthma attack decreases functional respiratory capacity we 
see excess carbon dioxide accumulating in the system.  This 
is, by definition, a respiratory acidosis.  It is not at all 
uncommon to find a respiratory acidosis pattern upon testing 
these patients with NUTRI-SPEC.  You must understand, however, 
that this respiratory acidosis is the result of, not the cause 
of the asthma.

     The problem with this respiratory acidosis of which we 
must be aware is that to compensate for the respiratory 
acidosis the patient dumps chlorides into the urine.  This 
loss of chlorides is very significant in asthma patients 
because it can tend to create a metabolic alkalosis or a 
dysaerobic imbalance.  It turns out that metabolic alkalosis 
and the dysaerobic imbalances resulting from the loss of 
chlorides can subsequently further stimulate the vagus nerve.  
This triggers the whole cycle all over again.

     Since asthma is always associated with a parasympathetic
bronchial tree, all of your patients with true asthma should 
test as parasympathetic on NUTRI-SPEC testing.  Many do --
however, some do not.  We are about to explain the reasons why 
some asthma patients do not test as parasympathetic -- but up
                            - 3 -

front you must understand that you will treat virtually all 
your asthma patients as parasympathetic.  You will never treat 
an asthma patient as sympathetic, no matter if their 
NUTRI-SPEC tests seem to indicate a sympathetic imbalance.  
Furthermore, since any respiratory acidosis imbalance is 
secondary to the asthma and treating it can push a person into 
a rebound chloride deficient stimulation of the vagus nerve --
you will never treat an asthma patient as a respiratory 

     Now, let us look at the reasons why many of your asthma 
patients with a parasympathetic condition do not test with 
NUTRI-SPEC as a parasympathetic imbalance, and may 
occasionally test as a sympathetic imbalance.

     One reason why some of your asthma patients will test 
sympathetic is simply because they are so heavily medicated.  
Most asthma medications are powerfully anti-parasym-
pathetic (which explains why they are effective).  With 
chronic use of these anti-parasympathetic medications the 
patient will begin to show an elevated blood pressure, an 
accelerated pulse, an exaggerated clinostatic pulse response, 
and an exaggerated orthostatic blood pressure response.  They 
will often also show an enlarged pupil and a white 
dermographics line.  In other words, they will show a classic 
sympathetic test pattern.  You must understand that this 
pattern is the result of the medication only, and that it is 
the pattern you want the patient to show.  As long as they are 
testing somewhat sympathetic their asthma symptoms are being 
controlled to some degree.

     If you make the mistake of treating an asthma patient as 
sympathetic as per a drug-induced sympathetic test pattern, 
you will push them directly back into an extreme state of 
parasympathetic imbalance and precipitate an asthma attack.  
Again, never treat an asthma patient as sympathetic.

     If you are going to treat your asthma patients as 
parasympathetic despite a sympathetic test pattern, how are 
you going to monitor their progress?  Most often there is at 
least one test in these patients that will still show a 
parasympathetic tendency.  Focus on this test as a means to 
monitor the patient.  The other very effective way to monitor 
the progress of these patients is with the test listed near 
the bottom of your Sympathetic/Parasympathetic QRG page --


Key into this as your best monitor of your asthmatic patients' 
progress.  You want to keep this number well above 2, and 
preferably closer to 3.  If this pulse pressure divided by the
                            - 4 -

respiratory rate quotient drops to 2 or less you know the 
patient is in trouble.  This indicator is your best overall
monitor of the status of your asthmatic patients.

     There is another reason why some of your asthmatic 
patients do not test parasympathetic and may even test as 
sympathetic.  If you look at the history of asthma over the 
last 40 years you find that two things have happened -- first, 
the incidence of asthma has increased dramatically; second, 
asthma, a condition that once was principally a childhood 
affliction that decreased or disappeared by the time a person 
reached adulthood, is now persisting throughout life and is 
even affecting many members of the adult population who did 
not suffer asthma as children.

     What has happened over the last 40 years to create the 
increase in frequency and duration of asthma?  This increase
has been shown to be associated with the immunization of 
children and the indiscriminate use of antibiotics in 

     Historically, asthma was found in patients who had an 
inborn tendency to a parasympathetic metabolic imbalance.  
Now, because of the influence of immunizations and 
antibiotics, we have patients who do not have a systemic 
parasympathetic tendency, but rather a localized 
parasympathetic tendency in the specific neurological control 
of the bronchial tree.  There is a possibility that the 
neurotoxic effect of vaccines damages an autonomic nerve 
ganglion which causes the localized parasympathetic 
over-reactivity and thus the asthma.  While this has not been 
proved conclusively, a study published in The Journal of 
Anthroposophic Medicine demonstrated that the recovery from 
childhood diseases plays a role in the maturation of the 
immune system and helps the individual develop resistance to 
disease, including helping to prevent the development of 
asthma and other chronic diseases.

     Another study published in Science showed that childhood 
infections paradoxically protect against asthma, and that 
allowing respiratory ailments to run their course is essential 
to developing natural immunity.  Suppressing this immune 
response leads to a state of neuro-immunological deficiency in 
the upper respiratory tract and a predisposition to asthma.

     So, to summarize, many of our modern day asthma 
conditions are associated with a localized parasympathetic  
over-reactivity rather than a systemic parasympathetic 
imbalance.  To control the asthma in these patients you must 
still treat them with Complex P, tyrosine, and very often with 
magnesium chloride as per your QRG.  However, you must be
                            - 5 -

cautious because these patients can very easily be pushed into 
a systemic state of sympathetic imbalance even as their
bronchial system is struggling with its own parasympathetic 
condition.  Use your pulse pressures divided by the respira-   
tory rate as a means to guide your clinical intervention.

     One other note on your asthmatic patients is that many of 
these people also tend to be anaerobic.  This imbalance can 
also be hidden by asthma medications, many of which push a 
patient more dysaerobic.  Look for an anaerobic tendency in 
these patients and treat it with Oxygenic A, Oxygenic A+, 
tyrosine, and methionine.

     While you will be of tremendous help to your asthma 
patients, most of them will continue to need some 
pharmacological intervention, at least from time to time.  
Which medications are the most beneficial and which ones are
damaging?  The best medications for your asthma patients are 
those which are both anti-parasympathetic and anti-anaerobic.  
These are the epinephrine analogs.  Most of them are provided
in the form of inhalers.  These constitute the most logical 
choice for asthma medication since they not only directly 
impact the symptom but are also addressing the underlying 
biochemical imbalances.

     While your epinephrine analogs are an excellent choice, 
theophylline is a good choice in those patients that are 
parasympathetic -- but is not good in those patients who have 
an anaerobic component to their asthma.

     The third common medication used for asthma is 
glucocorticoids.  These steroids are a very poor choice in 
that while they may give short term relief, they actually 
exacerbate the parasympathetic and the anaerobic imbalances 
that cause the asthmatic condition.  We could condone the use 
of the medication for short-term crisis relief despite its 
side effects if there were no other alternative.  However, 
since epinephrine is just as effective or more so at 
controlling an asthmatic crisis, there is no justification for 
using the steroids.

     In a crisis situation, such as when a severe asthma 
attack necessitates hospital emergency care, a shot of 
epinephrine (adrenalin) should be the first treatment choice.  
This used to be standard practice, but has been replaced by 
the use of prednisone.  Prednisone "works" symptomatically by 
virtue of its anti-inflammatory and anti-prostaglandin effect, 
while actually exacerbating the patient's underlying 
parasympathetic (and anaerobic) tendency.  Only asthmatics 
with a dysaerobic tendency derive more short-term good than
long-term harm from steroids.
                            - 6 -

     Two additional comments on asthma medications are in 
order.  First, many asthma medications and allergy medications 
contain sodium benzoate.  It has been found that this common 
cough, cold, and allergy medication actually causes asthma in 
many patients.  A study published in The Archives of 
Pediatrics showed that children with asthma had their 
condition clear completely as soon as they discontinued sodium 
benzoate containing medication.

     Finally, let us consider allergy shots, which are often 
used in the belief that a decreased sensitivity to an allergen 
would decrease the frequency or severity of asthma attacks.  I 
love it when establishment researchers set out to prove 
themselves right and end up stubbing their toe in the process.  
A study published in the New England Journal Of Medicine, 
which was designed to prove the efficacy of allergy shots in 
asthma patients, proved exactly the opposite.  When the study 
showed absolutely no benefit to allergy shots the researchers 
were dumbfounded, and in their state of disbelief urged 
caution in accepting their own study's conclusions.

     So -- what will you do with your next asthma patient?  
First, identify all their NUTRI-SPEC fundamental imbalances.  
Second, treat all those imbalances plus a parasympathetic 
imbalance regardless of whether the patient tests as parasym-
pathetic.  To monitor that patient use whatever tests they 
have that lean toward the parasympathetic side, plus 
particularly use the pulse pressures divided by the 
respiratory rate.  Finally, put the patient on the 
prostaglandin dietary recommendations in addition to the 
NUTRI-SPEC Fundamental Diet.  This means this patient must 
strictly avoid salad dressings, margarine, mayonnaise, nuts 
and nut butters, and all fried foods.  The patient should also 
be following the Parasympathetic Diet, which means a decrease 
in carbohydrate intake with particular attention to decreasing 
fruit and other forms of sugar, plus strict avoidance of 

     Your only additional responsibility with these patients 
is to check their medications.  Make sure they are taking no
sodium benzoate containing medications.  Also make sure that 
if they are using an inhaler it is an epinephrine analog and 
not a steroid.

     We are almost out of space for this Letter so let us 
squeeze a very big topic into a very small space.

                            - 7 -

     Some of your most difficult patients to balance 
metabolically are those who test both glucogenic and 
sympathetic, and those who test both ketogenic and parasym-
pathetic.  Much of what you do for one of these imbalances
can exacerbate the other.  What is going on here, anyway?

     Consider your patients who are both glucogenic and 
sympathetic.  The big picture here is not difficult to 
understand.  Your glucogenic patients have a strong tendency 
to be hypoglycemic.  With glucogenic forces pushing a person's 
body chemistry into a state of low blood and brain sugar, how 
will the body respond?  If the patient has an ounce of 
strength in their sympathetic system they will mobilize their 
sympathetic reserves in a desperate attempt to maintain blood 
sugar.  This is good to a point -- it shows that the patient 
is capable of mounting a compensatory adaptative stress 
response.  However, when the glucogenic hypoglycemic stress is 
unrelenting, the compensatory sympathetic response becomes 
habituated and in itself becomes a problem for these patients 
-- and cannot be ignored.

     Your QRG protocol does a pretty good job of 
distinguishing those glucogenic patients who have a 
sympathetic stress response that has gotten out of control.  
You must treat both imbalances simultaneously.  You must 
explain to the patient that they are going to be a problem 
case, and why.  And you must monitor that patient closely, 
being prepared to adjust the dosage of their glucogenic and 
sympathetic supplements according to the changes in their test 
pattern.  Very often one of these imbalances will correct very 
quickly, leaving the other as the major.

     Next, consider your patients who are both ketogenic and 
parasympathetic.  Here is the life story of most of these 
patients.  They began as a parasympathetic type during 
childhood.  They responded to excess dietary carbohydrate in 
typical parasympathetic fashion with a huge out pouring of 
insulin.  The large quantities of insulin pulled all the sugar 
out of their bloodstream causing a reactive hypoglycemia.  
These people rode the blood and brain sugar roller coaster for 
years through childhood and adolescence and early adulthood.

     After years of excess insulin production in response to 
excess carbohydrate the patient began to become somewhat 
insulin insensitive.  Now, in a state of dysinsulinism, the 
patient still puts out tremendous amounts of insulin in 
response to ingested carbohydrate, but now the insulin is no 
longer effective at pulling the sugar out of the blood.  The 
blood sugar levels now remain normal to somewhat high but are
accompanied by elevated insulin levels.
                            - 8 -

     The excess insulin levels are responsible for the 
ketogenic test pattern that you are now seeing.  The patient 
still has a systemic parasympathetic tendency, but is 
suffering from a ketogenic imbalance in regard to glycemic 
control.  The excess insulin levels set them up for even more 
pathology than the original parasympathetic tendency did.

     If this dysinsulinism persists over a number of years 
(and particularly if the patient becomes overweight on a diet 
of excess carbohydrate) this patient will become a Type II 
adult onset diabetic.  At that point in time the patient will 
probably no longer test as parasympathetic but as ketogenic 
only.  So, be aware that some of your ketogenic patients will, 
after being treated as ketogenic, show up as parasympathetic 
and you will need to change your therapeutic regimen.        

     But the patient that shows both ketogenic and 
parasympathetic right up front, you know you are catching them 
at a stage of life when they are just making the transition 
from a pure parasym- pathetic hypoglycemic type to a 
dysinsulinism ketogenic type.  Again, you must treat both 
imbalances; you must tell the patient that they are going to 
be a pain in the neck; and you must monitor them very closely 
-- being prepared to change your nutrition regimen as their 
objective tests change.

    This has been a most important Letter.  You were given 2 
extra pages to be absolutely certain:

- You have a thorough understanding of asthma, and how with 
NUTRI-SPEC you can consistently (and often dramatically) help 
your asthma patients by correcting the fundamental causes of 
their pathology.

- You have the expertise to analyze and effectively treat the 
patients who, up until now, have been driving you crazy -- 
those who test as both glucogenic and sympathetic, and as both 
ketogenic and parasympathetic.  The first thing to do with 
these patients is to tell them their "metabolic history" from 
childhood to present.  (They will be amazed at your 
perception.)  Let them appreciate why the are a special case 
and that you will be monitoring them very closely.  (Patients 
love to be special.)

     Put this information to work for you and your patients.  
No one else even understands what is going on in these 
patients, let alone can help them as you can with NUTRI-SPEC.

			   Guy R. Schenker, D.C.


Nutri-Spec Letters